further observations on contralateral remote masking and related phenomena

Received 15 May 1967 4.3, 4.4.5, 4.7, 4.15

Further Observations on Contralateral Remote Masking and Related Phenomena

W. D•xo• WARD

Hearing Research Laboratory, Department of Otolaryngology, University of Minnesota, Minneapolis, Minnesota 55455

Previous knowledge is reviewed relevant to contralateral remote masking (CRM)--the elevation in threshold of a low-frequency sinusoid in the presence of a high-frequency band of noise in the opposite ear--and a ser:es of additional observations is presented. CRM is nearly as great (1) in ears with paralyzed middle-ear muscles as in normal ears, (2) for bone-conducted as for air-conducted test tones, or (3) when a 50-msec tone pulse occurs simultaneously with the onset of the masking pulse as when it is presented half a second later. Further- more, (4) the gradual decrease of CRM with time, in the presence of a sustained masker, is not affected by abrupt changes in frequency or level of the masker, and (5) only a low negative correlation between CRM and auditory fatigue exists. These facts all indicate that the middle-ear muscles play only a minor role in CRM. The course of adaptation of CRM is shown to parallel the course of development of perstimulatory fatigue. It appears, therefore, that CRM represents primarily central masking arising at one or more centers receiving afferent innervation from both right and left ears, and that the change in time of CRM can be ascribed to adaptation processes either in the noise channel or, via the efferent system, in the contralateral channel. Implications of this formulation in regard to auditory fatigue from diotic and dichotic exposure to noise is discussed.

F a steady high-frequency noise whose intensity exceeds 85 dB SPL (dB re 0.0002 dyn/cm 2) is presented to one ear of a normal listener, the threshold for a low-frequency tone in the other is elevated. Such contralateral remote masking (CRM) might represent any one or a combination of (1) an attenuation of the test signal caused by reflex contraction of the middle- ear muscles (MEM), (2) direct masking by physiological noise from these muscles, or (3) some form of central masking' interaction between neural events originating at the respective cochleas.

I. CRM AND THE AURAL REFLEX

An earlier study of CRM (Ward, 1961a) led me to the conclusion that the reflex was more heavily involved than central masking. However, there soon appeared evidence that this decision was quite wrong, and that, instead, most of the threshold shift must be attributed to central factors. First, both Fletcher and King (1963), and Bilger (1966) showed that CRM can be observed in persons whose stapedius muscles had been excised; although the amount of CRM produced by a given noise is not as great as in normals, this may be due to the presence of a slight conductive deficit in the non- stapedectomized (contralateral) ears, which reduces the

sound reaching the cochlea and so decreases the central masking.

Similarly, persons with Bell's palsy, a disease whose symptoms include paralysis of the MEM, demonstrate just as much CRM as do normals. Figure 1 shows an example of this. The solid line represents the average CRM at 500 cps (250-msec test pulses) 30 sec after onset of a 1200-2400-cps noise whose level is given on the abscissa, for a group of 26 normal ears. The filled circles represent CRM when the noise was presented to the normal (left) ear of a man with Bell's palsy on the right

o 20 •

/o

8o 90 ioo •io i2o

SPL (DB)

Fro. 1. Contra]atera! remote masking (CRM) at .500 cps 30 sec after onset of 1200-2•00-cps no•se as a function of the SPL of the noise. •' average of 26 normal ears. O' •n LE, noise •n •E, of •nd•v•dua] w•th Bell's palsy on right s•de. •' CE• in RE, no•sc •n LE, same •nd•v•dua].

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W. D. WARD

side, the open circles represent the CRM with noise in the right ear. If anything, there is slightly more CRM of a tone on the affected side than on the normal side.

The same equivalence of results on normal and affected sides was found for two other Bell's palsy patients.

Apparently, then, the state of the MEM is, to a considerable extent, irrelevant to the occurrence of CRM. Before concluding that CRM has no bearing whatsoever on MEM action, however, it might be worthwhile to review the observations already published in regard to CRM, and to present some newer data on the topic.

II. PREVIOUS RESULTS

Earlier studies (Burgeat and Hirsh, 1961; Ward, 1961 a) disclosed the following characteristics of CRM:

(1) CRM caused by a steady noise decreases with time, generally reaching an asymptote after 3 to 5 min, at least for noises above 1200 cps; a later study (Ward, 1962a) showed that CRM at 250 cps induced by 600- 1200-cps noise continued to decrease for at least 20 min. On the other hand, Fletcher and Loeb (1962) found no change in CRM with time when a series of clicks was the masker.

(2) This decrease with time is equal to the decrease with time of the ipsilateral remote masking caused by the same high-frequency noise. For example, if a noise produced a CRM at 500 cps of 15 sec after onset and 10 dB 120 sec after onset, and also produced a remote masking in the noise ear of 55 dB at 15 sec, then the ipsilateral remote masking would drop to 50 dB at 120 sec.

(3) CRM (in decibels) grows linearly with SPL for SPL's above 90 dB, though at a rate less than unity.

(4) However, this growth with SPL depends on the frequency of the arousal noise; the higher the frequency, the slower the rate of growth of CRM.

(5) Nevertheless, extrapolation of such linear growth curves implies that CRM begins at about 85 dB SPL regardless of arousal frequency. Figure 2 illustrates some of the foregoing generalizations. Here, CRM at 500 cps produced by a 2400-4800-cps noise is shown as a function of SPL; time since onset is the parameter. At

3O

9 8 •ø

•o

8 o 80 90 I00 I10 120 130

SPL OF 2400-4800 NOISE

Fzo. 2. Relations between CRM and SPL as a function of time since onset of the noise (parameter).

30 sec, the rate of growth of CRM in this case is 0.54 dB/dB, beginning at 87 dB SPL.

(6) In general, CRM is greater at 500 cps than at 250 or 1000 cps.

(7) A high-frequency pure tone, even at 130 dB SPL, produces only 1 to 2 dB of CRM.

(8) There are large individual differences, not only in the SPL at which CRM begins, but also in the slope of the curve relating CRM to level. For example, with a masker of 2400-4800 cps, the SPL at which CRM at 500 cps began ranged from 77 to 101 dB in a group of 14 listeners, and the rate of growth of CRM with masker level varied from 0.28 to 0.75.

(9) However, there is no correlation between such individual differences (in intercept and slope) and differences in resting threshold at either the masker or maskee frequency.

(10) A brief interruption in the masker does not restore CRM to its original level. Although the CRM induced by repeated 1-min exposures to 2400-4800-cps noise at 115 dB SPL was constant when 30 sec of

rest was inserted between the exposures, a 15-sec interval resulted in progressively less CRM on successive tests.

(11) CRM is slightly greater when the test ear has just been exposed to the high-frequency noise (Ward 1961a, Fig. 2).

III. BONE CONDUCTION

Six additional experiments have been performed in order to elucidate the nature of CRM. The first three

of these utilized the apparatus and procedures described earlier (Ward, 1961a), and were reported orally several years ago (Ward, 1961b). The first experiment demon- strated that the threshold of a bone-conducted tone is

elevated by a contralateral noise to the same extent as an air-conducted tone. In addition to earphones, listeners wore a bone oscillator on the vertex. A 2400-

4800-cps noise at 110 dB SPL was delivered via one earphone to the less sensitive ear (the ear other than the one to which a 500-cps bone-conducted test tone was lateralized in quiet). The CRM was measured alternately via air and bone conduction (without moving the headphones) in 14 experienced listeners. For a bone-conducted tone, the CRM was 15.6, 13.1, and 11.3 dB at 15, 30, and 60 sec after onset of the noise, respectively, while the air-conducted tone shifted by 14.7, 12.0, and 9.6 dB, respectively. None of these differences between bone and air were significant; furthermore, the correlation coefficient between air and bone CRM was 0.76--that is, the same listeners who showed the most CRM via air also showed the most via bone.

IV. EFFECT OF CHANGES IN FREQUENCY AND LEVEL

The second study showed that switching from one frequency of masker to another does not restore the

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CONTRALATERAL REMOTE MASKING

CRM to the value it would have had, in the fresh ear, with the second noise. Two illustrative experiments are summarized in Fig. 3. The CRM at 500 cps was measured for 2 min in 15 listeners under four conditions'

(1) masking during first minute by crossed-filter noise at 1800 cps and 119 dB SPL, second minute by crossed-filter noise at 3600 cps and 121 dB SPL (left panel, solid circles); (2) the reverse of (1); (3) first minute 1200-2400-cps noise at 119 dB, second 4800- 9600 at 118 dB (right panel, solid circles); and (4) the reverse of (3). It is clear that the first minute had a profound effect on the CRM produced during the second minute of exposure to a different frequency (but at the same frequency). The left panel shows, for example, that the CRM produced by 1800-cps crossed filters after 1 min of preadaptation to 3600-cps crossed filters is just about the same as that expected if the preadaptation had been to 1800 itself.

Similarly, a third experiment showed that merely changing the level of the noise did not restore initial conditions either. The CRM at 500 cps produced by 2400-4800-cps noise at 100, 110, and 120 dB SPL was measured in 14 listeners under two conditions' (1) with 1 min of rest between exposures at successively higher levels, and (2) with no break at all. In Fig. 4, the solid lines designate the CRM measured with the intervening l-rain recovery periods, the dashed lines the CRM when the three exposures were juxtaposed.

In both of these experiments, the outcome is quite different from what would be expected if the MEM were responsible for the CRM. After continued exposure to a sustained stimulus, the muscles relax, but again contract when the exposure frequency is shifted by more than an octave (LQscher, 1930; Wers•ill, 1958), or when the intensity is raised by as little as 3 dB (Gjaevenes and S6hoel, 1966).

Also illustrated in Fig. 4 is the 1- to 2-dB "residual" contralateral threshold shift that persists for a minute or so after the exposure. In my experience, such residual shifts are always this small, although Loeb and Fletcher

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-- o3600X TO 1800X

01200-2400 TO 4800-9600 o4800-9600 TO 1200-2400

0.25 05 i 2 0.2:5 0.5 I 2

TIME SINCE ONSET OF FIRST NOISE (MIN)

f:•o. 3. Change of CRM at 500 cps as a function of time since onset of noise, for successive 1-min exposures to different noises having spectral widths of approximately { oct (left panel) or t oct (right panel). See text.

•o • •'ø!- •oo 0 / •'•

• I I I I I • o o I o i o I

TIME SINCE ONSET OF NOISE (MIN)

Fro. 4. Course of CRM at 500 cps produced by successive 1-min exposures to 2400-4800-cps noise at increasing levels (parameter). ..... no interval between exposures. -' 1-min rest between exposures.

(1961) report values of 7-8 dB at 500 cps following a 3-min exposure to 2000-2200-cps noise at 100 dB SL in the other ear.

V. CRM AND TTS

The fourth set of data OB_ CRY{ arose as a by-product of an intensive study of individual differences in temporary threshold shift (TTS) produced by various noises in a group of 49 young normals. The CRM at 500 cps was _measured for exposures at successively higher intensities to 1200-2400- and 2400-4800-cps noises. Specific procedures and some results have been reported elsewhere (Ward, 1966). In general, the earlier observations were substantiated' the growth with level at a rate less than unity; the change with time; and the lack of dependence on threshold sensitivity, either at the maskeror at the test frequency. In addition, two other conclusions were extracted from the data.

(1) The correlation between CRM produced in the two ears of a given listener was only about 0.50, although the test-retest correlation on a given ear for identical tests given six months apart was about 0.75. (2) Only small, though statistically significant, negative correlations were obtained between CRM in a

given ear and the TTS later produced by low-frequency tones and noises in the same ear. These correlation

coefficients had a median value of about --0.35, which _means that only slightly more than 10% of the between- individuals variance in TTS can be explained in terms of CRM. These values lie between those of Loeb and

Fletcher (1961), who reported no significant correlations, and those of Cohen et al. (1966), who found rank-order correlation coefficients of about -0.6

between CRM at 500 cps produced by 1200-2400-cps noise and TTS at 1000, 1500, 2000, and 3000 cps produced by a 15-rain exposure at 110 dB to a noise with maximum energy in the octave bands centered at 500 and 1000 cps. Such a negative correlation is a cogent indication that the MEM play at least a small part in CRM; the ears showing the most CRM tend to show less TTS when exposed to a low-frequency noise, as would be expected if they had more effective muscles.

The Journal of the Acoustical Society of America 595


W. D. WARD

VI. HIGH-FREQUENCY MASKING

In the study just described, measurements were also made of the opposite kind of CRM from that discussed heretofore--viz., the masking of a high-frequency test tone by a low-frequency noise in the other ear. In the present case, a 6700-cps test tone and a 125- dB-SPL 700-1400-cps masking noise were used. The mean threshold shift was 8 dB, with individual values ranging from -3 to 16 dB. This type of CRM also showed a small negative correlation with the TTS at 4 and 5.6 kc/sec produced by 15-min exposures to 1400-2800-cps noise; the ears showing the most TTS displayed the least high-frequency contralateral masking. However, it must be mentioned that, unlike the situation for the CRM at low frequencies produced by a high-frequency noise, this shift showed no significant decrease during the 1-min exposure period.

VII. CRM IN SHORT NOISE BURST

The fifth set of experiments, like the first three, were conducted before I had lost my conviction that the MEM were heavily involved in CRM. Previous experiments had shown that although the stapedius muscle begins to contract a few milliseconds after onset of a loud sound (Perlman and Case, 1939), the attain- ment of full reflex strength takes much longer (Metz, 1951). If an intense tone is to be effective in reducing the TTS produced by high-intensity clicks, its onset must precede the click by as much as 150 msec in some ears (Ward, 1962b). Furthermore, impedance measurements indicate that as much as a full second may be required for relaxation of the muscles. If one is listening to loud clicks in an anechoic room, one can often hear a soft "kuh" sound a fraction of a second after the click--a sound I have assumed to indicate the end of contraction.

Therefore, it seemed reasonable to assume that if one presents a low-frequency tone pip to one ear and a high-frequency noise burst to the other, the amount of contralateral threshold shift should depend on the exact temporal relations between the stimuli. Speci- fically, it was predicted that if the consensual aural reflex were able to produce a shift in threshold by reducing the amount of low-frequency energy reaching the cochlea, such an effect should require somewhere near 100 msec to build up to a maximum. A somewhat longer time should be needed for the shift to disappear.

By means of standard Tektronix pulse-generation equipment controlling two electronic switches, it was possible to manipulate the temporal relations between a high-intensity noise burst of a given duration and a 50-msec test tone pulse of 500 cps. Both stimuli had rise and fall times of 10 msec (so the "50-msec tone pulse" actually had a duration at peak intensity of only 30 msec). Each of 13 listeners adjusted the test tone to "just barely audible" by means of a switch controlling the "stepped" mode of operation of a

-I00 0 I00 200 300 400 500 600

TIME (MSEC)

Fro. 5. Ipsilateral (open points) and contralateral (filled points) remote masking of a 50-msec 500-cps tone burst by a 1200-2400- cps noise burst at 110 dB S?L. The beginning of the 500-msec noise burst is taken as zero on the abscissa; points are plotted at the midpoint (in time) of the test pulse.

Grason-Stadler recording attenuator; in this mode, throwing a toggle switch in one direction or the other increased or decreased, respectively, the test signal level by 1 dB. A stimulus pair was presented every 2.5 sec.

Figure 5 shows the ipsilateral and contralateral threshold shifts at 500 cps associated with 500-msec 110-dB-SPL bursts of 1200-2400-cps noise as a function of relative position of the tone pulse. The shift is plotted at the middle of the time interval concerned; for example, the shift of a tone pip that began just at the end of the masker is plotted at 525 msec, even though it began at 500 msec, rose to maximum intensity at 510 msec, and began decaying at 540 msec.

There is only a hint of an increase in the threshold as the position of the test pip was changed from 25 msec (onset coincident with onset of the noise) to 425 msec, and this is quite insignificant statistically (8 of the 13 listeners showed more shift at 425 msec than at 25, and 5 showed less). Surely there is not the change of 10 dB or more that one would expect if only reflex activity were responsible for the contralateral masking.

Thus, there seems to be scant evidence that contraction of the MEM causes a change in the transmission of low-intensity stimuli commensurate with the amount of reduction in the effectiveness of high-intensity stimuli they are known to provide. The hypothesis stated by Loeb and Riopelle (1960) becomes steadily more attractive; the notion that the reflex acts as an energy-limiting device, some sort of peak clipper, rather than as a resistive attenuator.

VIII. CRM AND PERSTIMULATORY FATIGUE

In the earlier article (Ward, 1961a), it was noted that the change of CRM with time bears at least a super- ficial resemblance to the course of "perstimulatory fatigue"--the gradual loss of ability of a stimulus sustained in one ear, to influence the lateralization of a

5c)6 Volume 42 Number 3 1967



...15

0 :30 60 90 120

TIME SINCE ONSET (SEC)

n • 0

• I0 ---•

Fro. 6. Changes in CRM (left ordinate and filled points) and perstimulatory fatigue (right ordinate and open points) produced by a steady 1200-2400-cps band of noise at 110 dB SPL, as a function of time since onset.

diotic test tone. Accordingly, the sixth experiment here was designed to compare CRM and perstimulatory fatigue (PERSF) under the same conditions.

Six experienced listeners were tested for both CRM at 500 cps and for PERSF to the noise itself during separate 2-min exposures to 1200-2400-cps noise at 100 dB SPL. Degree of PERSF at approximately 30-sec intervals after onset of the noise in one ear was

determined by introducing the noise to the other ear (the earphones were wired so that the signals were in phase), and instructing the listener to adjust an attenuator to give either "equal loudness" or "in the center of the head," whichever he preferred. Speed was stressed, in an attempt to minimize the effect of the growth of PERSF in the comparison ear that begins as soon as it is turned on. Four 2-min runs, with 2 min of rest intervening, were conducted for each of the 12 ears, as well as two runs measuring only CRM. Median individual settings for each time since onset were determined, and the average of these 12 medians calculated.

The results are shown in Fig. 6. The solid line and closed circles indicate the course of CRM (left ordinate); the values are about the same as those previously obtained for a larger group. The open circles represent the degree of PERSF (right ordinate). Since 8 to 10 sec was typically required by the listener to make the median plane lateralization (or equal-loudness balance), the averages have been plotted at 40, 70, 100, and 130 sec; also the two sets of data have been matched by making the assumption that CRM at the onset of the noise (i.e., at the same time that PERSF is zero) would have been 21.5 dB, as an extrapolation backwards in time from the data of Fig. 6 seems to imply. The similarity of the curves is obvious.

At first glance, it might appear that the mystery of the change of CRM with time is solved. When the "central effectiveness" of the noise decreases by X dB, as indicated by the growth of PERSF, the amount of contralateral masking of a 500-cps tone decreases by exactly the same amount. It would be tempting, therefore, to conclude that PERSF and CRM arise at exactly the same place. However, a little reflection will reveal that the exact congruence of the two curves must

be fortuitous. In the first place, since 10 sec were required to complete the adjustment, the measured PERSF will be something less than the true PERSF existing at the moment the noise is presented to the comparison ear. Furthermore, if the test tone had been some other frequency, say 250 cps instead of 500 cps, both the CRM and the change in CRM with time would have been smaller [-the ratio of CRM at 250 cps to that at 500 cps was found to be 0.67 at any given time, whether produced by 1200-2400- or 2400-4800-cps octave-band noise or by 1800- or 3600-cps crossed- filter noise (Ward, 1961a)•.

IX. DISCUSSION

It is hard to believe, nevertheless, that remote masking and PERSF do not have some common basis. Unfortunately, even if they do we are probably only trading one black box for another, for we seem to know about as little regarding PERSF as we do about CRM. Models typically presented to account for PERSF, although adequately embracing ipsilateral effects from exposures of up to 100 dB SPL, have no provision for effects on the other ear of sustained exposure. That is, it is usually assumed that in PERSF, changes in the auditory system occur only on the stimulated side, and that no effects of the exposure per se, other than those attributable to transcranial conduction of the sound, can be expected in the contralateral system. To be specific, such models (e.g., Small, 1963) postulate that the percentage of neural elements in the stimulated ear that are firing gradually decreases with prolonged exposure; therefore, when the other ear is presented with the same signal, the "normal" excitation from this ear will be more potent than the decreased activity on the stimulated side. The possibility has been suggested, however, although never taken very seriously before, that the neural response on the contralateral side may sometimes be enhanced by the exposure, so that when the new lateralization balance is made, the indicated PERSF arises not only from the diminution of neural activity on the stimulated side but also from an increase (over the normal condition) on the contralateral side (Wright, 1959).

You will note that I have refrained from calling perstimulatory fatigue measurements "loudness bal- ances." This was quite deliberate. Despite the pre- valence of such statements as this: "When submitted

to a sustained acoustic stimulation with both pure tones and noises man gets the experience that, after listening for a few minutes to the sound, its loudness seems to diminish" (Witrich, 1966), the fact of the matter is that such a subjective diminution is seldom reported. When I, for example, listen to a sustained 500- cps tone of 110- or 120-dB SPL, it seems to me to get louder; not until I add the same tone to the other ear am I aware that something has happened to make it less effective in some sense or other. One need not rely

The Journal of the Acoustical Society of America $97


W. D. WARD

merely on introspective evidence for this conclusion, however: Pikler and Harris (1960), in their studies of loudness tracking, have shown that a listener can maintain the intensity of a tone at a constant value for long periods of time using an attenuator that he adjusts in order to counteract slow changes of level introduced by the experimenter. If PERSF represented a decrease in the "absolute" loudness of a sustained tone, then the listeners should allow the tone to gradually drift up- ward in intensity, but they do not. Thus, although PERSF may properly be termed "adaptation," it is not, in the ordinary sense, loudness adaptation.

By analogy, then, we may reasonably argue that changes in CRM may reflect not only an adaptation process in the auditory system beginning with the ear receiving the high-intensity noise, but also some different adaptation process in the contralateral system. If so, CRM could arise in any or all of the elements of the auditory pathway at which reasonably direct connections between ipsilateral and contralateral centers exist.

Let us for a moment consider the origin of the inter- fering masking products. The first source that suggests itself consists of the distortion products generated at the cochlea receiving high-intensity noise, particularly the low-frequency components apparently de- rived from envelope detection (Deatherage et al., 1957). If we were to postulate that it is such distortion products that are adapting, in a manner implied by the change in time of CRM (recall that the same temporal change is seen in ipsilateral remote masking), the outcome of the second and third studies becomes quite reasonable. This is particularly true for the results obtained when the exposure noise frequency is shifted, as in Fig. 3. If adaptation is occurring to those elements of the distortion products in the 500-cps region, it will apparently proceed at the same pace, whether the distortion is produced by one noise band or another.

The main shortcoming of this formulation is that the ipsilateral masking produced by such distortion does not appear to be great enough to account for the degree of CRM we actually observe. Let me recapitulate some of the data from the earlier report (Ward, 1961a; especially Fig. 1) to illustrate the point. A 2400-4800- cps noise at 110 dB SPL generates, 30 sec after onset, an ipsilateral masking of 47 dB at 500 cps. This same 47 dB of masking is produced by an ipsilateral 70-dB band at the test-tone frequency (i.e., 300-600 cps) in young normal listeners. We might postulate, therefore, that the envelope detection products in the noise ear due to the 2400.4800-cps noise create the same dis- turbance in the cochlea, at the 500-cps region of the basilar membrane, as a "real" low-frequency noise of 70 dB SPL. However, a 70-dB-SPL 300-600-cps noise in one ear generates only 3 dB of ordinary central

masking of a $00-cps tone in the other. Therefore, the CRM from the 2400-4800-cps noise, one would expect, should also be only 3 dB. Instead, it is about 12 dB. Thus, the high-frequency noise must have an additional effect on the other auditory channel. Indeed, it was this discrepancy that originally led me to conclude-- erroneously, it is now clear--that the middle-ear muscles must have been producing 9 dB of effective attenuation in such a case.

A second objection to regarding the envelope detection products as being primarily responsible for CRM is that narrow-band noise (• oct) is just as effective as octave-band noise in producing CRM at 250 or 500 cps, despite the fact that its envelope contains con- siderably fewer components in that frequency region. That is, the width of the masking noise band seems to be irrelevant; the CRM is apparently a function only of the over-all level and the low-frequency cutoff (see Fig. 6 of Ward, 1961a). And yet, a pure tone produces no appreciable CRM at all! The arousal stimulus must fluctuate somewhat, but need not, it appears, do so at a modulation rate that includes the contralateral test

frequency. It is also perhaps worth noting here that if CRM were

solely a function of distortion, one would expect a positive, rather than a negative, correlation between remote masking, either ipsilateral or contralateral, and TTS. That is, a particularly high CRM would indicate a high level of distortion, which would imply either that the ear concerned was unusually sensitive or that it overloaded at unusually low levels; in either case, one would expect, if anything, more TTS.

If, then, the MEM are only slightly implicated in CRM, and if envelope detection products cannot account for the remainder, the high-frequency noise and/or its low-frequency distortion products must "feed over" to the other side at other stations along the auditory system. It is difficult to determine the most likely location for such a pre-emption of pathways. However, it will be recalled from Fig. 5 that CRM of a 50-msec tone pulse appears immediately. The absence of a latent period not only rules out the MEM but also argues against an explanation in terms only of the most peripheral elements of the chain, or for that matter, any neural circuit involving centrifugal fibers as the source of CRM (although the efferent system may well be involved in the change of CRM with time). If, for example, cochleo-cochlear inhibition were solely responsible, a delay of action of at least 30 msec would be expected (Grubel et al., !964), and the CRM should, therefore, be less at the beginning of the noise pulse than later. [-Of course, one might argue that the latency of such cochleo-cochlear action is balanced by some aspect of the on effect, such as "overshoot" (Zwicker, 1965); however, one should be most wary of explana-




tions that involve antagonistic action and a resulting cancellation of two forces, both of which are poorly understood!-[ But until electrophysiological studies of CRM at high intensities are undertaken, we can only speculate on the exact locus of the interference-- whether it occurs at the accessory nucleus of the superior olivary complex [thought at present to be the most peripheral center that receives afferent innervation from both ears--see Deatherage (1966) for a summary of the problem of binaural interaction in general-], or at higher centers such as the inferior colliculus or roedial geniculate, or perhaps at all of them.

X. CRM AND TTS

These studies of CRM suggest that we should re- examine the question of TTS from diotic and dichotic exposure. Two years ago, I was convinced that the prop- erties of the MEM were sufficient to account for all

of the differences between TTS's produced by monaural and binaural exposures (Ward, 1962c, 1965). In the case of a monotic versus diotic exposure to either a 1400-cps pure tone or a 700-1400-cps noise, a decreased TTS observed in the diotic condition could be ascribed

to a greater reflex contraction engendered by the greater loudness of the diotic exposure. Exposure to a broad- band noise gave a similar difference at low test frequencies, but there was much less difference at high frequencies, as one would expect if, as has been es- tablished indirectly, reflex muscle contraction attenu- ates only the low frequencies (below 2000 cps).

This formulation was also consistent with the

demonstration that the TTS produced by a 700-cps pure tone, but not by a 2000-cps pure tone, was much diminished when a narrow-band noise at the same fre-

quency was simultaneously presented to the other car. In this case, the supposition was that the time- varying nature of the noise kept the reflex aroused to a much greater extent than when the tone alone was presented.

These results led to the prediction that if one simultaneously fatigued one ear with a low-frequency tone and the other with a high-frequency band of noise, the TTS produced by the low-frequency tone should be diminished (relative to the monotic TTS) while the TTS from the high-frequency noise should be unaffected. Accordingly, this hypothesis was tested on 17 listeners using 5-min exposures of 700-cps tone at 115 dB SPL and 2400-4800-cps noise at 112 dB SPL, respectively. The results are shown in Fig. 7. The average TTS.o in both instances was reduced by 2.7 dB in the dichotic condition--apparently the low-frequency tone had just as much effect on the contralateral high-frequency neural elements as the high-frequency noise had on the contralateral low-frequency ones. It is possible that the diminution of TTS2 at high frequencies occurred only by chance (only 11.5 of the 17 listeners showed less TTS in the dichotic condition, which is not even

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Fro. 7. Comparison of temporary threshold shifts 2 min after 5-rain exposures to a 700-cps tone at 115-dB SPL (left) and a 2400-4800-cps noise at 112-dB SPL (right). Solid curves and filled circles indicate shifts following monotic exposure, open circles and dashed lines the shifts following diotic exposure (tone to one ear, noise to the other).

significant at the 10% level); but if the indicated mean proves to be correct, then other hypotheses must be sought to account for the results. At the moment, the same "efferent gunk" [-if I may borrow Wernick and Tobias's (1963) term-] that may possibly be involved in the gradual reduction of CRM with time seems as likely a suspect as any.

xI. SUMMARY

A group of experiments designed to elucidate the nature of CRM has resulted in a picture as thoroughly muddled as one finds in most areas of binaural inter-

action. Apparently the CRM at 500 cps produced by a high-frequency band of noise represents a combination of effects' (1) a slight reduction in the sound reaching the test ear, caused by contraction of the middle-ear muscles; (2) central masking by low-frequency distortion products originating at the cochlea of the noise ear; and (3) additional central interference between the massive neural activity in the noise-ear channel and the 500-cps test tone in the other, at any center receiving afferent innervation from both sides. It is also possible that the efferent system may be heavily involved, particularly in the process responsible for the gradual diminution of CRM with time. Since this rules out practically nothing, it is clear that, as usual, further research is indicated. At least, electrophysiological research is badly needed, although perhaps the psycho- physical evidence merely requires a more astute analysis than the present one.

ACKNOWLEDGMENT

This research was supported in full by grants from the Public Health Service, U.S. Department of Health, Education, and Welfare.

The Journal of the Acoustical Society of America 500


W. D. WARD

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further observations on contralateral remote masking and related phenomena

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